Atopic Dermatitis Challenge Center

The patient is empirically diagnosed with AD and eczema herpeticum. A Tzanck smear is done and is positive for multinucleate giant cells with nuclear molding and ballooning degeneration of the keratinocytes. 

Eczema herpeticum, or Kaposi varicelliform eruption, is a rare but potentially life-threatening complication of AD. It is an extensive cutaneous vesicular eruption that arises from pre-existing skin disease — in most cases, AD — and is caused by disseminated cutaneous viral infection, usually with the herpes simplex virus (HSV). The virus can infect the epidermis because of the skin barrier defects that are inherently associated with AD. Patients with AD and filaggrin gene null mutations may have an increased risk for eczema herpeticum. 

Eczema herpeticum is associated with significant morbidity and is considered a medical emergency. Early diagnosis and treatment is essential to prevent or minimize complications. Complications of eczema herpeticum can include keratoconjunctivitis, which may lead to vision loss, as well as multiorgan involvement with meningoencephalitis and/or septic shock. 

Eczema herpeticum occurs on areas of preexisting AD (or other skin disease) and presents as small, dome-shaped, grouped papule-vesicles on an erythematous base. When these vesicles rupture, punched-out ulcers are formed. It is seen most often on the face, neck, and upper trunk. Fever, malaise, and lymphadenopathies may also be present. 

Among patients with severe or poorly controlled AD, even the classic presentation of eczema herpeticum can be challenging to recognize. Clinicians should maintain a high index of suspicion for this complication in any patient with AD who presents with an acute pruritic and painful rash, including pediatric patients, who have the highest risk for the development of eczema herpeticum.

Viral PCR on vesicle fluid can confirm the diagnosis of eczema herpeticum and determine the type of HSV with high sensitivity and specificity. If unavailable, a Tzanck smear of an opened vesicle or erosion can confirm an HSV infection and provide rapid diagnosis, but its sensitivity and specificity can vary. Direct fluorescence antigen testing is a fast and inexpensive method for detecting an HSV antigen and distinguishing between HSV-1 and HSV-2 infections. Bacterial cultures should be performed when there is a concern for impetiginization. A skin biopsy may be indicated in cases involving atypical presentation. 

Immediate treatment with oral acyclovir should be initiated for any patient with eczema herpeticum; patients with severe disease or who are immunocompromised may require hospitalization for administration of systemic antivirals. Because secondary bacterial infections are common, prophylactic antibiotics (eg, cephalexin, clindamycin, doxycycline, or trimethoprim-sulfamethoxazole) may also be indicated. Finally, consultation with an ophthalmologist is indicated when herpes keratitis is suspected. 

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is empirically diagnosed with AD and eczema herpeticum. A Tzanck smear is done and is positive for multinucleate giant cells with nuclear molding and ballooning degeneration of the keratinocytes. 

Eczema herpeticum, or Kaposi varicelliform eruption, is a rare but potentially life-threatening complication of AD. It is an extensive cutaneous vesicular eruption that arises from pre-existing skin disease — in most cases, AD — and is caused by disseminated cutaneous viral infection, usually with the herpes simplex virus (HSV). The virus can infect the epidermis because of the skin barrier defects that are inherently associated with AD. Patients with AD and filaggrin gene null mutations may have an increased risk for eczema herpeticum. 

Eczema herpeticum is associated with significant morbidity and is considered a medical emergency. Early diagnosis and treatment is essential to prevent or minimize complications. Complications of eczema herpeticum can include keratoconjunctivitis, which may lead to vision loss, as well as multiorgan involvement with meningoencephalitis and/or septic shock. 

Eczema herpeticum occurs on areas of preexisting AD (or other skin disease) and presents as small, dome-shaped, grouped papule-vesicles on an erythematous base. When these vesicles rupture, punched-out ulcers are formed. It is seen most often on the face, neck, and upper trunk. Fever, malaise, and lymphadenopathies may also be present. 

Among patients with severe or poorly controlled AD, even the classic presentation of eczema herpeticum can be challenging to recognize. Clinicians should maintain a high index of suspicion for this complication in any patient with AD who presents with an acute pruritic and painful rash, including pediatric patients, who have the highest risk for the development of eczema herpeticum.

Viral PCR on vesicle fluid can confirm the diagnosis of eczema herpeticum and determine the type of HSV with high sensitivity and specificity. If unavailable, a Tzanck smear of an opened vesicle or erosion can confirm an HSV infection and provide rapid diagnosis, but its sensitivity and specificity can vary. Direct fluorescence antigen testing is a fast and inexpensive method for detecting an HSV antigen and distinguishing between HSV-1 and HSV-2 infections. Bacterial cultures should be performed when there is a concern for impetiginization. A skin biopsy may be indicated in cases involving atypical presentation. 

Immediate treatment with oral acyclovir should be initiated for any patient with eczema herpeticum; patients with severe disease or who are immunocompromised may require hospitalization for administration of systemic antivirals. Because secondary bacterial infections are common, prophylactic antibiotics (eg, cephalexin, clindamycin, doxycycline, or trimethoprim-sulfamethoxazole) may also be indicated. Finally, consultation with an ophthalmologist is indicated when herpes keratitis is suspected. 

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is empirically diagnosed with AD and eczema herpeticum. A Tzanck smear is done and is positive for multinucleate giant cells with nuclear molding and ballooning degeneration of the keratinocytes. 

Eczema herpeticum, or Kaposi varicelliform eruption, is a rare but potentially life-threatening complication of AD. It is an extensive cutaneous vesicular eruption that arises from pre-existing skin disease — in most cases, AD — and is caused by disseminated cutaneous viral infection, usually with the herpes simplex virus (HSV). The virus can infect the epidermis because of the skin barrier defects that are inherently associated with AD. Patients with AD and filaggrin gene null mutations may have an increased risk for eczema herpeticum. 

Eczema herpeticum is associated with significant morbidity and is considered a medical emergency. Early diagnosis and treatment is essential to prevent or minimize complications. Complications of eczema herpeticum can include keratoconjunctivitis, which may lead to vision loss, as well as multiorgan involvement with meningoencephalitis and/or septic shock. 

Eczema herpeticum occurs on areas of preexisting AD (or other skin disease) and presents as small, dome-shaped, grouped papule-vesicles on an erythematous base. When these vesicles rupture, punched-out ulcers are formed. It is seen most often on the face, neck, and upper trunk. Fever, malaise, and lymphadenopathies may also be present. 

Among patients with severe or poorly controlled AD, even the classic presentation of eczema herpeticum can be challenging to recognize. Clinicians should maintain a high index of suspicion for this complication in any patient with AD who presents with an acute pruritic and painful rash, including pediatric patients, who have the highest risk for the development of eczema herpeticum.

Viral PCR on vesicle fluid can confirm the diagnosis of eczema herpeticum and determine the type of HSV with high sensitivity and specificity. If unavailable, a Tzanck smear of an opened vesicle or erosion can confirm an HSV infection and provide rapid diagnosis, but its sensitivity and specificity can vary. Direct fluorescence antigen testing is a fast and inexpensive method for detecting an HSV antigen and distinguishing between HSV-1 and HSV-2 infections. Bacterial cultures should be performed when there is a concern for impetiginization. A skin biopsy may be indicated in cases involving atypical presentation. 

Immediate treatment with oral acyclovir should be initiated for any patient with eczema herpeticum; patients with severe disease or who are immunocompromised may require hospitalization for administration of systemic antivirals. Because secondary bacterial infections are common, prophylactic antibiotics (eg, cephalexin, clindamycin, doxycycline, or trimethoprim-sulfamethoxazole) may also be indicated. Finally, consultation with an ophthalmologist is indicated when herpes keratitis is suspected. 

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is diagnosed with atopic dermatitis (AD) on the basis of clinical findings and historical features, morphology and distribution of skin lesions, and associated clinical signs.

AD continues to be a clinical diagnosis. Pruritus and eczema (acute, subacute, or chronic) are essential features for the diagnosis of AD. The eczema should follow characteristic morphology and age-specific patterns (eg, facial/neck/extensor involvement in children, flexural involvement in any age group, sparing of the groin and axillary regions). A personal or family history of atopy is an important historical feature that supports the diagnosis of AD, as are xerosis and early age of onset.

The majority of patients with AD (60%) develop symptoms during the first year of life and 90% experience an eruption by 5 years of age, but disease onset can occur at any age. Some studies have found an association between late-onset AD and persistence of disease into adulthood.

At present, there are no reliable biomarkers that can differentiate AD from other entities. An elevated total and/or allergen-specific serum IgE level is the most commonly associated laboratory feature, but it is not seen in about 20% of individuals with AD. Additionally, elevated allergen-specific IgE levels are found in 55% of the general population in the United States, making it nonspecific for AD. Moreover, while total IgE level usually varies in accordance with disease severity, it is not a reliable marker of disease severity, and it is possible for individuals with severe disease to have normal levels. Nonatopic conditions (eg, parasitic infection, some cancers, and autoimmune disease) may also lead to elevations in IgE levels.

Consistent prognostic markers are also lacking, although elevated total serum IgE levels and filaggrin gene null mutations do tend to be predictive of a more severe and prolonged disease course.

Topical agents including nonpharmacologic moisturizers and topical corticosteroids are the mainstay of treatment for AD; immunomodulatory agents and targeted biologic therapies are also available. For patients with more severe or recalcitrant disease, systemic therapy or phototherapy may be used, often in conjunction with topical therapies.

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is diagnosed with atopic dermatitis (AD) on the basis of clinical findings and historical features, morphology and distribution of skin lesions, and associated clinical signs.

AD continues to be a clinical diagnosis. Pruritus and eczema (acute, subacute, or chronic) are essential features for the diagnosis of AD. The eczema should follow characteristic morphology and age-specific patterns (eg, facial/neck/extensor involvement in children, flexural involvement in any age group, sparing of the groin and axillary regions). A personal or family history of atopy is an important historical feature that supports the diagnosis of AD, as are xerosis and early age of onset.

The majority of patients with AD (60%) develop symptoms during the first year of life and 90% experience an eruption by 5 years of age, but disease onset can occur at any age. Some studies have found an association between late-onset AD and persistence of disease into adulthood.

At present, there are no reliable biomarkers that can differentiate AD from other entities. An elevated total and/or allergen-specific serum IgE level is the most commonly associated laboratory feature, but it is not seen in about 20% of individuals with AD. Additionally, elevated allergen-specific IgE levels are found in 55% of the general population in the United States, making it nonspecific for AD. Moreover, while total IgE level usually varies in accordance with disease severity, it is not a reliable marker of disease severity, and it is possible for individuals with severe disease to have normal levels. Nonatopic conditions (eg, parasitic infection, some cancers, and autoimmune disease) may also lead to elevations in IgE levels.

Consistent prognostic markers are also lacking, although elevated total serum IgE levels and filaggrin gene null mutations do tend to be predictive of a more severe and prolonged disease course.

Topical agents including nonpharmacologic moisturizers and topical corticosteroids are the mainstay of treatment for AD; immunomodulatory agents and targeted biologic therapies are also available. For patients with more severe or recalcitrant disease, systemic therapy or phototherapy may be used, often in conjunction with topical therapies.

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is diagnosed with atopic dermatitis (AD) on the basis of clinical findings and historical features, morphology and distribution of skin lesions, and associated clinical signs.

AD continues to be a clinical diagnosis. Pruritus and eczema (acute, subacute, or chronic) are essential features for the diagnosis of AD. The eczema should follow characteristic morphology and age-specific patterns (eg, facial/neck/extensor involvement in children, flexural involvement in any age group, sparing of the groin and axillary regions). A personal or family history of atopy is an important historical feature that supports the diagnosis of AD, as are xerosis and early age of onset.

The majority of patients with AD (60%) develop symptoms during the first year of life and 90% experience an eruption by 5 years of age, but disease onset can occur at any age. Some studies have found an association between late-onset AD and persistence of disease into adulthood.

At present, there are no reliable biomarkers that can differentiate AD from other entities. An elevated total and/or allergen-specific serum IgE level is the most commonly associated laboratory feature, but it is not seen in about 20% of individuals with AD. Additionally, elevated allergen-specific IgE levels are found in 55% of the general population in the United States, making it nonspecific for AD. Moreover, while total IgE level usually varies in accordance with disease severity, it is not a reliable marker of disease severity, and it is possible for individuals with severe disease to have normal levels. Nonatopic conditions (eg, parasitic infection, some cancers, and autoimmune disease) may also lead to elevations in IgE levels.

Consistent prognostic markers are also lacking, although elevated total serum IgE levels and filaggrin gene null mutations do tend to be predictive of a more severe and prolonged disease course.

Topical agents including nonpharmacologic moisturizers and topical corticosteroids are the mainstay of treatment for AD; immunomodulatory agents and targeted biologic therapies are also available. For patients with more severe or recalcitrant disease, systemic therapy or phototherapy may be used, often in conjunction with topical therapies.

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.